Primary coronary angiography revealed 3-vessel coronary artery disease with concomitant severe ectatic malformation of coronary vessels. The culprit lesion was a subtotal stenosis of the proximal left anterior descending artery with reduced thrombolysis in myocardial infarction flow (Figure 3A). The proximal part of the circumflex artery had a 90% stenosis, and the proximal left obtuse marginal artery did as well (Figure 3A). In addition, a chronic total occlusion (CTO) was verified at the proximal right coronary artery (RCA; thrombolysis in myocardial infarction flow 0; Movie I in the online-only Data Supplement) with retrograde filling from the left posterolateral artery through epimyocardial collaterals to the right posterior interventricular artery (Figure 3B and 3C; Movie II in the online-only Data Supplement). Levocardiography revealed severe anterolateral and apical akinesia (ie, myocardial stunning), corresponding to a moderately reduced left ventricular ejection fraction (36%; Movie III in the online-only Data Supplement). Immediate percutaneous coronary intervention with the implantation of drug-eluting stents (DES) into the proximal left anterior descending artery (Xience Pro 3.5/23 mm, Abbott, Chicago, IL) and proximal circumflex artery (Xience Pro 4.0/28 mm, Abbott), and plain old balloon angioplasty of the proximal obtuse marginal artery, as well (Trek 2.0/20 mm Trek balloon, Abbott), was performed (Figure 3D). Dual-antiplatelet therapy was prescribed with aspirin 100 mg/d permanently and prasugrel 10 mg/d for 12 months. Computed tomography angiography excluded any further arterial arteriosclerotic involvements at the main branches of the thoracic aorta or pulmonary arteries. The patient fully recovered and was discharged after 7 days of in-hospital treatment.

Specifically addressing the prognostic benefit of a complete revascularization of 3-vessel coronary artery disease, elective percutaneous coronary intervention of RCA-CTO was planned. Dual-injection angiography using a 2 guide catheter strategy with a 6F extra backup 4.0 catheter with sideholes being placed at the left coronary artery via right radial access and a 7F Amplatz left 1 catheter with sideholes being placed at the RCA via right femoral access (ie, dual femoral–radial access), as well, proved good intermediate results after percutaneous coronary intervention with DES implantation into the proximal left anterior descending and circumflex arteries. Most notably, however, the former RCA-CTO lesion revealed spontaneous and complete antegrade revascularization with a resting 90% tandem stenosis at the proximal RCA (Figure 3E; Movie IV in the online-only Data Supplement). Final percutaneous coronary intervention with DES implantation was performed without any further complications (2 bare metal stents, Prokinetic 5.0/26 mm and 5.0/15 mm, Biotronik SE & Co.KG, Berlin Germany; Figure 3F).

CTOs represent the most challenging coronary lesions to treat, frequently left unrevascularized because of perceptions of high failure rates and technical complexity even in patients experiencing symptoms of coronary ischemia.1 However, in experienced centers, the success rates of interventional revascularization of >85% are reported (http://www.ercto.org/).1 A CTO lesion is defined by standard characteristics, which were also evident in the case reported here: (1) a large vessel diameter (in this case, proximal RCA, segment 1) before the proximal cap of the CTO lesion with minimal residual antegrade filling corresponding to an incompetent target coronary vessel at the distal cap; (2) an estimated lesion length >20 mm; (3) retrograde epimyocardial collateral circulation from the repaired donor vessel circumflex artery-posterolateral artery despite the large vessel diameter of the proximal RCA; and (4) persistent inferior hypokinesia in comparison with anteroseptal to apical akinesia 6 months after the initial ST-segment myocardial infarction.

To our knowledge, our case is the first description of spontaneous revascularization of a CTO lesion in a patient with concomitant TNF inhibitor treatment because of rheumatoid arthritis.

Several reports point out an increased incidence of coronary artery disease and increased cardiovascular mortality risk in rheumatoid arthritis.2 Increased plaques burden and severity is variably characterized by noncalcified, mixed, or fully calcified plaques and may result in obstructive or nonobstructive multivessel disease and in silent coronary ischemia, as well.3 However, evaluations of different diagnostic techniques to most reliably prove coronary artery disease involvement in rheumatoid arthritis (eg, coronary calcium score by computed tomography scan, invasive coronary flow reserve, etc) deliver controversial results. Accordingly, available data regarding the outcomes of acute coronary syndrome in rheumatoid arthritis are conflicting.

Treating rheumatoid arthritis with TNF inhibitors, such as adalimumab, is recommended in patients with a high disease activity (ie, Clinical Disease Activity Index >22 or Simplified Disease Activity Index >26) and refractory treatment response to combined methotrexate and prednisone at 3 months.2 TNF is a key cytokine-mediating effector pathway in both inflammatory disease target tissues and in atherosclerotic vessels.4 Treatment of inflammatory arthritis with TNF inhibitors additionally modulates vascular risk factors4 and has beneficial effects on vascular outcomes. These beneficial effects of TNF inhibitors toward arthrosclerotic lesions have been attributed to the modulation of endothelial cell function, the reduction of vascular stiffness, and the reduction of fibrinogen, homocysteine, and lipoprotein (a), as well.4

Therefore, it is conceivable to assume that these anti-inflammatory effects of the TNF inhibitor adalimumab might be the reason for the effects seen in our case. Accordingly, the patient reported about an improvement of typical clinical features of rheumatoid arthritis such as joint swelling and morning stiffness of hands and feet since the time of adalimumab treatment, and further improvement of cardiac exercise level being assessed by noninvasive spiroergometry was documented.

Highlighting the association of systemic inflammation in rheumatoid arthritis with an increased cardiovascular event and mortality risk, this case exemplarily represents severe extra-articular manifestation of coronary vasculitis. Treating relevant coronary lesions with DES in patients with systemic inflammatory arthritis or vasculitis has been described even with good long-term results. Accompanying prednisolone medication after stent implantation was shown to possibly lower the recurrence of angina pectoris. Whether or not the development of new coatings of DES with TNF inhibitors might lead to an improvement for this specific patient group remains unclear.

In conclusion, systemic inflammation leading to severe coronary vasculitis leading to ST-segment myocardial infarction can occur in patients with rheumatoid arthritis and should be included in the differential diagnosis. The use of TNF inhibitors could be considered as another pharmacological treatment option for an optimal treatment strategy in this subset of patients.

. 2012 update of the 2008 American College of Rheumatology recommendations for the use of disease-modifying antirheumatic drugs and biologic agents in the treatment of rheumatoid arthritis.Arthritis Care Res (Hoboken). 2012;64:625–639. doi: 10.1002/acr.21641.